Drugs online research references
Biol Pharm Bull. 1993 Jul;16(7):660-3.
Cardiomyopathic hamster hearts: long-term effects of drugs on catecholamine contents and binding characteristics of alpha 1- and beta 1-adrenergic receptors.
Watanabe K, Shibata A, Wakabayashi H, Shimada K, Sasaki K, Nagatomo T.
Division of Cardiovascular Research Laboratories, Tsubame Rosai Hospital, Niigata, Japan.
Changes were examined in myocardial catecholamine content and alpha 1- and beta 1-adrenoceptors during the development of cardiomyopathy in Syrian hamsters (Bio 14.6) and age-matched healthy controls. In addition, the effects of bunazosin, atenolol, xamoterol, ketanserin, and verapamil on the catecholamine content and [3H]prazosin, [3H]CGP12177 bindings to alpha 1- and beta 1-adrenergic receptors of myocardium were compared with those of the controls. (1) Lower norepinephrine and dopamine levels were observed in 35-week-old cardiomyopathic hamster hearts than in the controls. There was, however, a tendency for a slight decrease of alpha 1- and beta 1-adrenoceptors in cardiomyopathic hamsters. (2) Administration of bunazosin induced lower dopamine values in 18-week-old cardiomyopathic hamsters. (3) Xamoterol induced a higher Kd value for beta 1-adrenoceptors and lower dopamine content than for those with cardiomyopathy. Ketanserin also induced a higher Bmax value than for cardiomyopathy. Thus, drug treatments clearly change catecholamine content and binding characteristics of the adrenoceptors which play an important role in the development of cardiac hypertrophy and heart failure.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8104623&dopt=Abstract
Am Heart J. 1985 May;109(5 Pt 2):1145-50.
Immediate central hemodynamic effects of five different beta-adrenoceptor-blocking agents, acebutolol, atenolol, pindolol, practolol, and propranolol, in patients with ischemic heart disease.
Svendsen TL, Trap-Jensen J, Carlsen JE, McNair A.
The hemodynamic effects of acebutolol were studied in six patients with ischemic heart disease. The changes in heart rate, cardiac output, and arterial blood pressure were determined after intravenous administration of six increasing doses of acebutolol to a cumulative dose of 0.64 mg/kg. After the sixth dose of acebutolol, cardiac output and heart rate were reduced 15% and 8%, respectively. Pulmonary artery pressure was increased by 4 mm Hg. Arterial blood pressure was not changed significantly. The effects of graded doses of acebutolol on heart rate and cardiac output were compared with earlier obtained results after atenolol (0.19 mg/kg), pindolol (0.025 mg/kg), practolol (0.64 mg/kg), and propranolol (0.19 mg/kg). The effects of increasing doses of acebutolol and practolol were very similar and significantly different from the effects of the other three drugs in spite having been administered at equipotent doses. The hemodynamic effects of acebutolol support the hypothesis that the hemodynamic response to beta-adrenoceptor antagonist drugs at rest is determined primarily by the degree of intrinsic sympathomimetic activity, whereas beta-1 selectivity does not modify the central hemodynamic response.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2859778&dopt=Abstract
J Cardiovasc Pharmacol. 1988 May;11(5):552-63.
Pharmacological and hemodynamic profile of nebivolol, a chemically novel, potent, and selective beta 1-adrenergic antagonist.
Van de Water A, Janssens W, Van Neuten J, Xhonneux R, De Cree J, Verhaegen H, Reneman RS, Janssen PA.
Research Laboratories, Janssen Pharmaceutica, Beerse, Belgium.
The pharmacological profile of nebivolol (N), a chemically novel beta-adrenergic antagonist, was assessed in investigations on isolated tissues, awake spontaneously hypertensive rats (SHR), closed-chest anesthetized dogs, and humans. In vitro, N was found to be a potent antagonist of beta 1-adrenergic receptors (A2 value, 5.8 X 10(-9) M) and only a weak beta 2-adrenergic antagonist (A2 value, 1.7 X 10(-6) M). The selectivity for the beta 1-adrenergic receptor was higher for N than for any of the reference compounds. In dogs--similarly with atenolol--N was more potent in blocking the isoprenaline (I)-induced increases in left ventricular performance than the I-induced decrease in arterial pressure. In dogs, as compared with propranolol, N (0.025 and 0.01 mg.kg-1 i.v.) increased cardiac output and stroke volume, lowered systemic vascular resistance, and had no significant effect on the variables related to left ventricular contraction. In contrast to other beta-adrenergic antagonists, N acutely lowered arterial blood pressure in SHR (1.25 mg.kg-1 i.p.) and in hypertensive patients (1 oral dose of 5 mg) for several hours. In healthy volunteers N (5 mg) lowered systemic vascular resistance during daily oral treatment and did not negatively affect left ventricular function. In conclusion, N is a potent and selective beta 1-adrenergic blocking agent with an interesting hemodynamic profile. In hypertensive subjects and SHR, a single dose lowers arterial blood pressure for substantial periods of time.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2455841&dopt=Abstract
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